High-temperature responses of Myzus persicae and its parasitoid Aphidius gifuensis in relation to heat level, duration and developmental stage.

BACKGROUND: Understanding how parasitoids respond to temperature is crucial for improving biological control strategies under the context of global warming. This study examined the suitability of Myzus persicae and its parasitoid Aphidius gifuensis to varying temperature conditions, as well as the stage-specific response of A. gifuensis to high temperatures. RESULTS: High temperatures had a significant impact on the both M. persicae and A. gifuensis. When exposed to 36°C, M. persicae developed more slowly and produced smaller adults compared to control, regardless of the duration of exposure (2, 4 or 6 h); additionally, the survival rate of M. persicae nymphs sharply decreased under these conditions. Exposure to 36°C for 4 h negatively impacted the development of A. gifuensis. Female parasitoids exposed to 32°C developed into smaller adults, whereas males exposed to all three temperature levels were smaller compared to control group. Female parasitoids exposed to high temperatures, regardless of the specific heat level and duration, exhibited reduced longevity and decreased fecundity. None of the parasitoids exposed to 36°C for 6 h daily developed into adults. Heat treated during early developmental stages (2 and 4 days old) had a greater influence on parasitoid development, whereas heat treatment at 4 and 6 days old had a more significant impact on its fecundity. CONCLUSION: High temperatures not only directly affected the performance of A. gifuensis, but also exerted indirect effects by influencing the quality of the host aphids M. persicae. The deleterious effects of high temperature on larvae can persist into the adult stage, affecting the longevity and reproduction of adults. These findings are important for the utilization of A. gifuensis in the control of M. persicae in warming environments. © 2024 Society of Chemical Industry.

Predicting the potentially exacerbation of severe viral pneumonia in hospital by MuLBSTA score joint CD4 + and CD8 +T cell counts: construction and verification of risk warning model.

PURPOSE: This study mainly focuses on the immune function and introduces CD4+, CD8+ T cells and their ratios based on the MuLBSTA score, a previous viral pneumonia mortality risk warning model, to construct an early warning model of severe viral pneumonia risk. METHODS: A retrospective single-center observational study was operated from January 2021 to December 2022 at the People's Hospital of Liangjiang New Area, Chongqing, China. A total of 138 patients who met the criteria for viral pneumonia in hospital were selected and their data, including demographic data, comorbidities, laboratory results, CT scans, immunologic and pathogenic tests, treatment regimens, and clinical outcomes, were collected and statistically analyzed. RESULTS: Forty-one patients (29.7%) developed severe or critical illness. A viral pneumonia severe risk warning model was successfully constructed, including eight parameters: age, bacterial coinfection, CD4+, CD4+/CD8+, multiple lung lobe infiltrations, smoking, hypertension, and hospital admission days. The risk score for severe illness in patients was set at 600 points. The model had good predictive performance (AUROC = 0.94397), better than the original MuLBSTA score (AUROC = 0.8241). CONCLUSION: A warning system constructed based on immune function has a good warning effect on the risk of severe conversion in patients with viral pneumonia.

Application of Bioactive Materials for Osteogenic Function in Bone Tissue Engineering.

Bone tissue defects present a major challenge in orthopedic surgery. Bone tissue engineering using multiple versatile bioactive materials is a potential strategy for bone-defect repair and regeneration. Due to their unique physicochemical and mechanical properties, biofunctional materials can enhance cellular adhesion, proliferation, and osteogenic differentiation, thereby supporting and stimulating the formation of new bone tissue. 3D bioprinting and physical stimuli-responsive strategies have been employed in various studies on bone regeneration for the fabrication of desired multifunctional biomaterials with integrated bone tissue repair and regeneration properties. In this review, biomaterials applied to bone tissue engineering, emerging 3D bioprinting techniques, and physical stimuli-responsive strategies for the rational manufacturing of novel biomaterials with bone therapeutic and regenerative functions are summarized. Furthermore, the impact of biomaterials on the osteogenic differentiation of stem cells and the potential pathways associated with biomaterial-induced osteogenesis are discussed.

Diagnostic performance of a multiplexed gastrointestinal PCR panel for identifying diarrheal pathogens in children undergoing hematopoietic stem cell transplant.

BACKGROUND: Diarrhea is a common complication of hematopoietic stem cell transplantation (HSCT) and is associated with substantial morbidity, but its etiology is often unknown. Etiologies of diarrhea in this population include infectious causes, chemotherapy- or medication-induced mucosal injury and graft-versus-host disease (GVHD). Distinguishing these potential causes of diarrhea is challenging since diarrheal symptoms are often multifactorial, and the etiologies often overlap in transplant patients. The objectives of this study were to evaluate whether the FilmArray gastrointestinal (GI) panel would increase diagnostic yield and the degree to which pre-transplantation colonization predicts post-transplantation infection. METHODS: From November 2019 to February 2021, a total of 158 patients undergoing HSCT were prospectively included in the study. Stool specimens were obtained from all HSCT recipients prior to conditioning therapy, 28 ± 7 days after transplantation and at any new episode of diarrhea. All stool samples were tested by the FilmArray GI panel and other clinical microbiological assays. RESULTS: The primary cause of post-transplantation diarrhea was infection (57/84, 67.86%), followed by medication (38/84, 45.24%) and GVHD (21/84, 25.00%). Ninety-five of 158 patients were colonized with at least one gastrointestinal pathogen before conditioning therapy, and the incidence of infectious diarrhea was significantly higher in colonized patients (47/95, 49.47%) than in non-colonized patients (10/63, 15.87%) (P < 0.001). Fourteen of 19 (73.68%) patients who were initially colonized with norovirus pre-transplantation developed a post-transplantation norovirus infection. Twenty-four of 62 (38.71%) patients colonized with Clostridium difficile developed a diarrheal infection. In addition, FilmArray GI panel testing improved the diagnostic yield by almost twofold in our study (55/92, 59.78% vs. 30/92, 32.61%). CONCLUSIONS: Our data show that more than half of pediatric patients who were admitted for HSCT were colonized with various gastrointestinal pathogens, and more than one-third of these pathogens were associated with post-transplantation diarrhea. In addition, the FilmArray GI panel can increase the detection rate of diarrheal pathogens in pediatric HSCT patients, but the panel needs to be optimized for pathogen species, and further studies assessing its clinical impact and cost-effectiveness in this specific patient population are also needed.

Discovery of natural multi-targets neuraminidase inhibitor glycosides compounds against influenza A virus through network pharmacology, virtual screening, molecular dynamics simulation, and in vitro experiment.

Influenza virus continually challenges both human and animal health. Moreover, influenza viruses are easy to mutate. In a certain degree, vaccines may not catch up with rapid mutant paces of viruses. Anti-influenza drugs NIs (neuraminidase inhibitors) are one of the best choices. Therefore, based on ADMET properties, eight optimal natural multi-targets NIs glycosides compounds (IC50 = 0.094-97.275 µM) are found from radix glycyrrhizae, flos sophorae, caulis spatholobi, radix astragali, radix glycyrrhizae, semen astragali complanati, and common fenugreek seed through network pharmacology, molecular docking, dynamics simulation, quantum chemistry, and in vitro experiment. Moreover, mechanism research illustrates these natural compounds treat influenza A virus through key targets TLR4, TNF, and IL6 (high fever, acute respiratory distress syndrome), MAPK1, and MAPK3 (MAPK signaling pathway, viral RNP export, and viral protein expression), IL1B (NOD-like receptor signaling pathway, suppressed maturation of pro-IL-1ß and pro-IL-18), CASP3 (apoptosis), AKT1 (inhibited premature apoptosis), and EP300 (viral myocarditis, chemoattraction of monocytes and macrophages, T-cell activation antibody response).

[Inhibitory effect and molecular mechanism of sinomenine on human hepatocellular carcinoma HepG2 and SK-HEP-1 cells].

This study aimed to investigate the effect and molecular mechanism of sinomenine on proliferation, apoptosis, metastasis, and combination with inhibitors in human hepatocellular carcinoma HepG2 cells and SK-HEP-1 cells. The effect of sinomenine on the growth ability of HepG2 and SK-HEP-1 cells were investigated by CCK-8 assay, colony formation assay, and BeyoClick~(TM) EdU-488 staining. The effect of sinomenine on DNA damage was detected by immunofluorescence assay, and the effect of sinomenine on apoptosis of human hepatocellular carcinoma cells was clarified by Hoechst 33258 staining and CellEvent~(TM) Cystein-3/7Green ReadyProbes~(TM) reagent assay. Cell invasion assay and 3D tumor cell spheroid invasion assay were performed to investigate the effect of sinomenine on the invasion ability of human hepatocellular carcinoma cells in vitro. The effect of sinomenine on the regulation of protein expression related to the protein kinase B(Akt)/mammalian target of rapamycin(mTOR)/signal transducer and activator of transcription 3(STAT3) signaling pathway in HepG2 and SK-HEP-1 cells was examined by Western blot. Molecular docking was used to evaluate the strength of affinity of sinomenine to the target cysteinyl aspartate specific proteinase-3(caspase-3) and STAT3, and combined with CCK-8 assay to detect the changes in cell viability after combination with STAT3 inhibitor JSI-124 in combination with CCK-8 assay. The results showed that sinomenine could significantly reduce the cell viability of human hepatocellular carcinoma cells in a concentration-and time-dependent manner, significantly inhibit the clonogenic ability of human hepatocellular carcinoma cells, and weaken the invasive ability of human hepatocellular carcinoma cells in vitro. In addition, sinomenine could up-regulate the cleaved level of poly ADP-ribose polymerase(PARP), a marker of apoptosis, and down-regulate the protein levels of p-Akt, p-mTOR, and p-STAT3 in human hepatocellular carcinoma cells. Molecular docking results showed that sinomenine had good affinity with the targets caspase-3 and STAT3, and the sensitivity of sinomenine to hepatocellular carcinoma cells was diminished after STAT3 was inhibited. Therefore, sinomenine can inhibit the proliferation and invasion of human hepatocellular carcinoma cells and induce apoptosis, and the mechanism may be attributed to the activation of caspase-3 signaling and inhibition of the Akt/mTOR/STAT3 pathway. This study can provide a new reference for the in-depth research and clinical application of sinomenine and is of great significance to further promote the scientific development and utilization of sinomenine.

Glycyrrhizin inhibits LPS-induced inflammatory responses in goat ruminal epithelial cells in vitro.

Inflammation plays a crucial role in the progression of Subacute Ruminal Acidosis (SARA). The experiment was designed to investigate anti-inflammatory effects of glycyrrhizin on goats ruminal epithelial cells (GREC) which were induced SARA by Lipopolysaccharide (LPS) in vitro. The GREC were induced SARA by adding LPS at the concentration of 5 µm and glycyrrhizin was added at different concentration of 0, 60, 90, 120, 150 µm. The structural integrity of LPS-induced GREC with the treatment of glycyrrhizin were observed by electron microscope; The levels of inflammatory factors TNF-α, IL-1ß, IL-6, IL-8 and IL-12 were measured by ELISA; The number of Zo-1 and Occludin were measured, the expression of tight junction protein Occludin were measured by Western blot, and the mRNA expression of NF-κB, TNF-α, IL-1ß, IL-6, IL-8 and IL-12 were measured in vitro. The results showed that higher concentration treatment of glycyrrhizin led to better morphology in LPS-induced GREC. Glycyrrhizin inhibited the growth of inflammatory factors TNF-α, IL-1ß, IL-6, IL-8 and IL-12 in a dose-dependent manner. The number of ZO-1 and Occludin increased with the increase of adding of glycyrrhizin. Western blot analysis showed that the expression of tight junction protein Occludin in LPS-induced GREC increased with the adding of glycyrrhizin in a dose-dependent manner. Furthermore, the mRNA expression of NF-κB, TNF-α, IL-1ß, IL-6, IL-8 and IL-12 decreased significantly with the increase treatment of glycyrrhizin. Glycyrrhizin significantly inhibits LPS-induced inflammatory mediators in GREC and the effects are better with the increase treatment of glycyrrhizin in vitro.

RB1 5́UTR contains an IRES related to cell cycle control and cancer progression.

Retinoblastoma gene1 (RB1) is the first tumor suppressor gene that stands as the guardian of the gate of the G1 period and plays a central role in proliferation and differentiation. However, no reports focused on the possible internal ribosome entry site (IRES) function of the RB1 gene flanking sequence. In this study, we constructed a bicistronic reporter with the RB1 5'untranslated region (5́UTR) inserted between two reporter coding regions. We found RB1 5'UTR harbors an IRES and has higher activity in cancer cell lines than normal cells. Besides, RB1 IRES acquired the highest activity in the G0/G1 phase of the cell cycle, and the RB1 5'UTR mutation collected from retinoblastoma decreased IRES activity compared with RB1 5'UTR wild-type. These data indicated that RB1 IRES is a mechanism of stress regulation and is related to cell cycle control and cancer progression.

Spinal cord injury: molecular mechanisms and therapeutic interventions.

Spinal cord injury (SCI) remains a severe condition with an extremely high disability rate. The challenges of SCI repair include its complex pathological mechanisms and the difficulties of neural regeneration in the central nervous system. In the past few decades, researchers have attempted to completely elucidate the pathological mechanism of SCI and identify effective strategies to promote axon regeneration and neural circuit remodeling, but the results have not been ideal. Recently, new pathological mechanisms of SCI, especially the interactions between immune and neural cell responses, have been revealed by single-cell sequencing and spatial transcriptome analysis. With the development of bioactive materials and stem cells, more attention has been focused on forming intermediate neural networks to promote neural regeneration and neural circuit reconstruction than on promoting axonal regeneration in the corticospinal tract. Furthermore, technologies to control physical parameters such as electricity, magnetism and ultrasound have been constantly innovated and applied in neural cell fate regulation. Among these advanced novel strategies and technologies, stem cell therapy, biomaterial transplantation, and electromagnetic stimulation have entered into the stage of clinical trials, and some of them have already been applied in clinical treatment. In this review, we outline the overall epidemiology and pathophysiology of SCI, expound on the latest research progress related to neural regeneration and circuit reconstruction in detail, and propose future directions for SCI repair and clinical applications.

Spinal cord injury-activated C/EBPß-AEP axis mediates cognitive impairment through APP C586/Tau N368 fragments spreading.

Spinal cord injury (SCI) leads to mental abnormalities such as dementia and depression; however, the molecular mechanism of SCI-induced dementia remains a matter of debate. Asparagine endopeptidase (AEP) mediated dementia by enhancing amyloid plaque and Tau hyperphosphorylation, indicating that it played an important role in neurodegeneration. Here we revealed that SCI stimulated AEP activation in mice with T9 contusion injury. Activated-AEP cleaved APP and Tau, resulting in APP C586 and Tau N368 formations, and consequentially accelerated Aß deposit and Tau hyperphosphorylation, respectively. At 9 months following injury, mice demonstrated a severe deterioration in cognitive-behavioral function, which was corroborated by the presence of accumulated AD-specific pathologies. Surprisingly, activated AEP was found in the brains of mice with spinal cord injury. In contrast, AEP knockout reduced SCI-induced neuronal death and neuroinflammation, resulting in cognitive-behavioral restoration. Interestingly, compared to the full-length proteins, truncated Tau N368 and APP C586 were easier to bind to each other. These AEP-processed fragments can not only be induced to pre-formed fibrils, but also amplified their abilities of spreading and neurotoxicity in vitro. Furthermore, as a critical transcription factor of AEP, C/EBPß was activated in injured spinal cord. Elevated C/EBPß level, as well as microglia population and inflammatory cytokines were also noticed in the cortex and hippocampus of SCI mice. These neuroinflammation pathologies were close related to the amount of Tau N368 and APP C586 in brain. Moreover, administration with the AEP-specific inhibitor, compound #11, was shown to decelerate Aß accumulation, tauopathy and C/EBPß level in both spinal cord and brain of SCI mice. Thus, this study highlights the fact that spinal cord injury is a potential risk factor for dementia, as well as the possibility that C/EBPß-AEP axis may play a role in SCI-induced cognitive impairment.

Combination therapy with ultrasound and 2D nanomaterials promotes recovery after spinal cord injury via Piezo1 downregulation.

Spinal cord injury (SCI) causes severe neurological dysfunction and currently has no effective treatment. Due to the complex pathophysiological processes associated with SCI and the limited efficacy of single strategies, the need for combined strategies for effective SCI therapy is becoming increasingly apparent. In this study, we evaluated the combined effects of layered double hydroxide-coupled NT3 (MgFe-LDH/NT3) nanoparticles (NPs) and ultrasound (US) both in vitro and in vivo. Combined treatment promoted neural stem cell (NSC) differentiation into neurons and exerted anti-inflammatory effects in vitro. Furthermore, combined therapy promoted behavioural and electrophysiological performance at eight weeks in a completely transected murine thoracic SCI model. Additional RNA sequencing revealed that ultrasonic-induced Piezo1 downregulation is the core mechanism by which combined therapy promotes neurogenesis and inhibits inflammation, and the Piezo1/NF-κB pathways were identified. Hence, the findings of this study demonstrated that the combination of ultrasound and functional NPs may be a promising novel strategy for repairing SCI.

Selective dechlorination degradation of chlorobenzenes by dual single-atomic Fe/Ni catalyst with M-N/M-O active sites synergistic.

Removal and detoxification of chlorobenzenes have attracted public concern, multiple active sites single-atom Fe and single-atom Ni composite nitrogen-doped graphene (FeSA/CN/NiSA) cathode catalyst supplied generation and adsorption capacity of hydrogen and hydroxyl active species. M-O active sites coupled with M-N improved activity and stability of the catalyst, and decreased bond breaking energy barrier of C-Cl, FeSA/CN/NiSA-NiF cathode showed superior removal performance of chlorinated aromatic hydrocarbons (monochlorobenzene: 98.9%, dichlorobenzene: over 90.4%, trichlorobenzene: over 85.7%) and selectivity. Chlorobenzenes were dechlorinated under low stepwise voltage on the FeSA/CN/NiSA-NiF cathode. The efficiencies of stepwise dechlorination reactions of chlorobenzenes were all above 76%, Faradaic efficiencies were above 71.8%. The FeSA/CN/NiSA-NiF cathode was not sensitive to the molecular structure and has overcome the high energy barrier of chlorobenzenes molecular structure. The electrophilic attack of H*ads formed hyperconjugation bond weakened the possibility of the Cl atom forming a bond with the benzene ring, and was favorable for the Cl position to achieve single-electron transfer dechlorination. The selective stepwise dechlorination degradation of chlorobenzenes by FeSA/CN/NiSA-NiF cathode with multiple active sites demonstrated the advantaged performance of M-O and M-N active sites coupled synergistic in electrochemical reduction and degradation, providing a strategy for product-selective degradation of chlorinated aromatic hydrocarbons.

Biocompatible exosome-modified fibrin gel accelerates the recovery of spinal cord injury by VGF-mediated oligodendrogenesis.

Exosomes show potential for treating patients with spinal cord injury (SCI) in clinical practice, but the underlying repair mechanisms remain poorly understood, and biological scaffolds available for clinical transplantation of exosomes have yet to be explored. In the present study, we demonstrated the novel function of Gel-Exo (exosomes encapsulated in fibrin gel) in promoting behavioural and electrophysiological performance in mice with SCI, and the upregulated neural marker expression in the lesion site suggested enhanced neurogenesis by Gel-Exo. According to the RNA-seq results, Vgf (nerve growth factor inducible) was the key regulator through which Gel-Exo accelerated recovery from SCI. VGF is related to myelination and oligodendrocyte development according to previous reports. Furthermore, we found that VGF was abundant in exosomes, and Gel-Exo-treated mice with high VGF expression indeed showed increased oligodendrogenesis. VGF was also shown to promote oligodendrogenesis both in vitro and in vivo, and lentivirus-mediated VGF overexpression in the lesion site showed reparative effects equal to those of Gel-Exo treatment in vivo. These results suggest that Gel-Exo can thus be used as a biocompatible material for SCI repair, in which VGF-mediated oligodendrogenesis is the vital mechanism for functional recovery.

Bioactive 2D nanomaterials for neural repair and regeneration.

Biomaterials have provided promising strategies towards improving the functions of injured tissues of the nervous system. Recently, 2D nanomaterials, such as graphene, layered double hydroxides (LDHs), and black phosphorous, which are characterized by ultrathin film structures, have attracted much attention in the fields of neural repair and regeneration. 2D nanomaterials have extraordinary physicochemical properties and excellent biological activities, such as a large surface-area-to-thickness ratio, high levels of adhesion, and adjustable flexibility. In addition, they can be designed to have superior biocompatibility and electrical or nano-carrier properties. To date, many 2D nanomaterials have been used for synaptic modulation, neuroinflammatory reduction, stem cell fate regulation, and injured neural cell/tissue repair. In this review, we discuss the advances in 2D nanomaterial technology towards novel neurological applications and the mechanisms underlying their unique features. In addition, the future outlook of functional 2D nanomaterials towards addressing the difficult issues of neuropathy has been explored to introduce a promising strategy towards repairing and regenerating the injured nervous system.

IFN-τ mediated miR-26a targeting PTEN to activate PI3K/AKT signalling to alleviate the inflammatory damage of bEECs.

Endometritis is the failure of embryo implantation and an important cause of infertility in dairy cows. IFN-τ is a type I interferon unique to ruminants. In regulating the process of inflammatory response, IFN-τ can be expressed through MicroRNAs (miRNAs) to regulate the process of inflammation. However, IFN-τ regulates lipopolysaccharide (LPS)-induced inflammatory injury of bEECs through the highly conserved miR-26a in mammals, and the mechanism remains unclear. Bovine endometrial epithelial cells (bEECs)were isolated and cultured to establish an inflammatory injury model. RT-qPCR and ELISA were used to detect the secretion of inflammatory factors. Dual-luciferase assays and target gene silencing assays determine the regulatory role of miRNAs. The target protein was detected by immunofluorescence and western blotting. This study showed that the expression of miR-26a was significantly down-regulated in mouse endometrium inflammatory injury tissue and LPS stimulated bEECs; and IFN-τ reversed the expression of miR-26a. The study also showed that the overexpression of miR-26a significantly inhibited the secretion of pro-inflammatory cytokines IL-1ß, IL-6 and TNF-α. In addition, studies have shown that miR-26a inhibits its translation by targeting PTEN 3'-UTR, which in turn activates the Phosphatidylinositide 3-kinases/protein kinase B (PI3K/AKT) pathway, so that nuclear factor kappa-B (NF-κB) signaling is inhibited. In summary, the results of this study further confirm that IFN-τ as an anti-inflammatory agent can up-regulate the expression of miR-26a and target the PTEN gene to inhibit the inflammatory damage of bEECs.

Reduced expression of lncRNA DLEU7-AS1 is a novel favorable prognostic factor in acute myeloid leukemia.

The objective of our study was to measure DLEU7-AS1 expression in de novo acute myeloid leukemia (AML) whilst also analyzing its clinical relevance. We used gene expression data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), Cancer Cell Line Encyclopedia (CCLE) and Genotype-Tissue Expression project (GTEx) to assess the expression profile of DLEU7-AS1 in pan-cancers, cancer cell lines and normal tissues. Reverse transcription-quantitative PCR was used to measure DLEU7-AS1 expression in bone marrow from 30 normal individuals and 110 patients with de novo AML. DLEU7-AS1 expression was found to be markedly reduced in the AML samples of the TCGA pan-cancer datasets. In our PCR validation, DLEU7-AS1 expression was significantly decreased in the AML samples compared with that in controls (P<0.001). Low DLEU7-AS1 expression (DLEU7-AS1low) correlated positively with lower blood platelet counts (P=0.029). In addition, low DLEU7-AS1 expression was more frequently observed in the intermediate (58%; 44/76) and favorable karyotypes (65%; 15/23) compared with that in the poor karyotype (10%; 1/10; P=0.005). In particular, patients with high expression levels of DLEU7-AS1 (DLEU7-AS1high) showed lower complete remission rates (P=0.002) than patients with DLEU7-AS1low. Survival analysis revealed that patients with DLEU7-AS1low had longer overall survival (OS) than patients with DLEU7-AS1high (P<0.05). Multivariate Cox analysis demonstrated that in patients with non-acute promyelocytic leukemia (non-M3) who were ≤60 years old, DLEU7-AS1 expression was an independent prognostic factor for OS. Furthermore, we found distinct correlations among the expression of DLEU7-AS1, infiltration by immune cells and immune checkpoint genes in AML.

Jamming attack against remote state estimation over multiple wireless channels: A reinforcement learning based game theoretical approach.

In this paper, we design a potential game to investigate the interplay between sensors and attackers in wireless remote estimation systems (RESs), where we consider both closed-loop and open-loop scenarios that depend on whether the sensor's actions are known to the attacker or not. As a typical application of Cyber-Physical Systems (CPSs), wireless RESs have been showing vulnerable to channel jamming attacks. As a countermeasure, the wireless sensor in the estimation system can switch to another independent wireless channel to transmit sensor data. However, a smart attacker can also switch the target channel to launch a jamming attack, resulting in a game between the sensor and attacker. Moreover, the reinforcement learning based methods are proposed to obtain solutions of the designed game models in two scenarios. We also provide extensive simulation results to validate the effectiveness of the proposed methods.

A new approach for reducing pollutants level: a longitudinal cohort study of physical exercises in young people.

BACKGROUND: The present study aimed to evaluate the elimination of three common pollutants (dimethoate, benzo(a)pyrene (BaP) and bisphenol A (BPA) by different physical exercises and to assess the possible factors which could affect the pollutants elimination. METHODS: A total of 200 individuals who chose different kinds of exercises in accordance to their own wish were recruited. The levels of urinary pollutants were measured using ß-glucuronidase hydrolysis followed by a high-performance liquid chromatography tandem mass spectrometry-based method. RESULTS: Totally, the levels of dimethoate, BaP and BPA were reduced after physical exercises. However, the elimination of BaP in male was higher than that in female but the elimination of BPA in female was higher than that in male. Multivariate logistic regression showed that the degree of heart rate (HR) change was a protective factor affecting the improvement effect of dimethoate, BaP and BPA while BMI (body mass index) was a risk factor. Nevertheless, sex was a risk factor affecting the improvement of dimethoate and BaP but had a lower efficacy on BPA improvement. CONCLUSION: The present findings indicate that physical exercises can be considered as a novel approach to eliminate pollutants level in human body and can also give suggestions for choosing specific physical exercises to male and female individuals. Moreover, those who are with higher BMI need to lose weight before eliminating pollutant level through physical exercises.

Study of the genus Torreya (Taxaceae) based on chloroplast genomes.

BACKGROUND: Species of the genus Torreya are similar in morphology, and their morphological taxonomic characteristics are not stable because of environmentally induced changes. Therefore, morphology is insufficient for understanding their relationships. Chloroplast genome sequencing technology provides a powerful tool for molecular analysis to get more infomation for classification and identification of Torreya genus. METHODS: A total of 4 chloroplast genome of Torreya, including T. Parvifolia, T. nucifera, T. fargesii var. Yunnanensis and T. grandis var. jiulongshanensis, were sequenced and annotated. Campartive genome and phylogenetic tree were provided for variation analysis. RESULTS: The chloroplast genome size of the four samples is about 137 kb, the inverted repeat (IR) regions are identified in the genus Torreya. Genome comparison using mVISTA showed high sequence similarity among different species. Regions with divergence in exon regions include accD, ndhB, ndhF, psbA, psbJ, rpl2, rps3, rps16, rps18, ycf1, and ycf2. The phylogenetic tree based on 73 single-copy genes showed a clearer relationships among different species of Torreya. CONCLUSIONS: All genomes of the four Torreya species consist of two short IR regions, and results of the phylogenetic analysis concluded that T. parvifolia should be considered as T. fargesii var. yunnanensis or treated as a sister species. T. grandis var. jiulongshanensis should be treated as a variety of T. grandis according to molecular evidence, supporting the originally published proposal.

The Up-regulation of TNF-α Maintains Trigeminal Neuralgia by Modulating MAPKs Phosphorylation and BKCa Channels in Trigeminal Nucleus Caudalis.

Trigeminal neuralgia (TN) is a severe chronic neuropathic pain. Despite numerous available medical interventions, the therapeutic effects are not ideal. To control the pain attacks, the need for more contemporary drugs continues to be a real challenge. Our previous study reported that Ca2+-activated K+ channels (BK Ca ) channels modulated by mitogen-activated protein kinases (MAPKs) in the trigeminal ganglia (TG) neurons play crucial roles in regulating TN, and some research studies demonstrated that inflammatory cytokine tumor necrosis factor alpha (TNF-α) could promote neuropathic pain. Meanwhile, the trigeminal nucleus caudalis (TNC), the first central site of the trigeminal nociceptive pathway, is responsible for processing sensory and pain signals from the peripheral orofacial area. Thus, this study is aimed to further investigate whether TNF-α and MAPKs phosphorylation in the TNC could mediate the pathogenesis of TN by modulating BK Ca channels. The results showed that TNF-α of the TNC region is upregulated significantly in the chronic constriction injury of infraorbital nerve (ION-CCI) rats model, which displayed persistent facial mechanical allodynia. The normal rats with target injection of exogenous TNF-α to the fourth brain ventricle behaved just like the ION-CCI model rats, the orofacial mechanical pain threshold decreased clearly. Meanwhile, the exogenous TNF-α increased the action potential frequency and reduced the BK Ca currents of TNC neurons significantly, which could be reversed by U0126 and SB203580, the inhibitors of MAPK. In addition, U0126, SB203580, and another MAPK inhibitor SP600125 could relieve the facial mechanical allodynia by being injected into the fourth brain ventricle of ION-CCI model rats, respectively. Taken together, our work suggests that the upregulation of TNF-α in the TNC region would cause the increase of MAPKs phosphorylation and then the negative regulation of BK Ca channels, resulting in the TN.